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SCAF1
-
SR-related CTD-associated factor 1

Homo sapiens

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Cloning of a gene (SR-A1), encoding for a new member of the human Ser/Arg-rich family of pre-mRNA splicing factors: overexpression in aggressive ovarian cancer[1].

The CTD of human SR-A1 protein (aa 1187-1312), containing a conserved CTD-interaction domain and bearing a decahistidine (His10) tag was produced by DNA recombinant overexpression techniques in Escherichia coli from the vector pET16b and it was localized in the periplasmic space [2].

To the best of our knowledge, this is the first study examining the expression of the novel gene SR-A1 in colon cancer progression [3].

High SR-A1 expression was observed in 31/81 (38.3%) breast cancer tissues and was found to be more frequent in patients with tumors of large size (p=0.027), as well as in lymph node-positive patients (p=0.035) [4].

Because all nucleotide changes in the mutants that disrupted SRA function were silent mutations presumed not to alter deduced encoded amino acid sequence, our analysis provides strong evidence that SRA-mediated coactivation is executed by distinct RNA motifs and not by an encoded protein [6].

These findings support a role for mildly oxidized LDL in the redox regulation of macrophage differentiation and SR-A expression and suggest that increased vascular oxidative stress may contribute to the formation of both SMC and macrophage foam cells[7].

Here we show that coincubation of SMC with macrophages or oxidized low density lipoproteins (LDL) from macrophage-conditioned medium activates these same regulatory pathways and stimulates SR-A expression [7].

Oxidative stress caused by phorbol esters or reactive oxygen up-regulates the class A scavenger receptor (SR-A) in human smooth muscle cells (SMC), which normally do not express this receptor [7].

Furthermore, the mRNA of the SR-A1 gene in these cell lines appears to increase by estrogens, androgens and glucocorticoids, and to a lesser extend by progestins [1].

Therefore, in the present study we examined the expression of the SR-A1 gene in colon cancer tissues by RT-PCR and found that it is overexpressed as compared to normal mucosa (p=0.01) [3].

Using these antisera we show that the expression of SR-A protein is induced during monocyte to macrophage differentiation and that SR-A mediates 80% of the uptake of acetylated low density lipoprotein by human monocyte-derived macrophages[9].

A specific and selective role for SR-A was shown, since bone marrow culture-derived Mphi from SR-A(-/-) mice ingested fewer E. coli organisms than did wild-type cells, while uptake of antibody-opsonized E. coli was unaffected [5].

In contrast, among a scavenger receptor family, IL-4 as well as histamine up-regulated U937 cells to express the LOX-1 gene but not the SR-A gene, which genes encode receptors that scavenge oxidized lipids [10].